RAS Inhibitors SG Flashcards

1
Q

When are ACE inhibitors very effective? What conditions might limit the responsiveness to ACE inhibitors?

A

Large response
- Pts with ↑ed RAS activation
Decreased response
- RAS suppression due to volume expansion: mineracortocid use, primary aldosteronism, eating a ton of licorice

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2
Q

Why do you tell HF pts NOT to take NSAIDs?

A

↑risk HF relapse!!!

Blocks PG synthesis - impt for renal compensation during HF

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3
Q

Drug interaction between ibuprofen and diuretics

A

Ibuprofen ↑Na load

Can ↓effectiveness of diuretic

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4
Q

Can HF pts take aspirin for antiplatelet use or no cause you said no NSAIDs?

A

Yes to baby aspirin - low dose is still beneficial as anti-platelet med
NO to aspirin doses for everyday pain
- Impair PG synthesis

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5
Q

Even though BBs are often use post-infarction, what is the risk/what pts might you not do this for?

A

Exacerbate chronic asthma

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6
Q

Why no RAS inhibitors for renal artery stenosis pts

A

Can cause renal faiure

↓AGT2 mediated efferent arteriole constriction + ↓renal BF = inadequate GFR

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7
Q

SE of ACE inhibitors

A

Dry cough

Angioedema - can happen anytime during therapy, when start or years after successful treatment

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8
Q

If HF pt complains of wet cough, should you take them off ACE inhibitors?

A

NO
Productive cough = volume overload
Not ACE inhibitor rxn

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9
Q

How do aldosterone levels change with ACE inhibitors?

A

+ ACE inhibitor
Initial ↓aldosterone
Escape for longterm HF –> ↑aldosterone which ↑risk CV remodeling
Long term management:
ACE inhibitor + mineralcorticoid receptor blocker

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10
Q

SE of spironolactone

A

Hyperkalemia
Male impotence
Female amenorrhea
↓chances by using eplerenone

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11
Q

Drug for pharm stress test

A

Dobutamine

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12
Q

What is neprilysin

A

inactivates natiuretic peptides

Possible drug target as you try to increase ANP

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13
Q

Neprilysin + ACE inhibitor or ARB?

A

Nep + ARB

Both Nep & ACE inhibitors have SE of angioeema

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